Download
glomerulonephritis n.
Skip this Video
Loading SlideShow in 5 Seconds..
Glomerulonephritis PowerPoint Presentation
Download Presentation
Glomerulonephritis

Glomerulonephritis

330 Views Download Presentation
Download Presentation

Glomerulonephritis

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

  1. Glomerulonephritis

  2. Introduction Definition : • This is a bilateral non suppurative proliferation and inflammation of the glomeruli 2ry to immunological injury. -Classification -Based on clinical course -Based on Aetiology -Based on Renal Biopsy morphology

  3. 1.Clinical Course -Acute glomerulonephritis: Prognosis is better, most show complete recovery. Few may progress to CRF & HTN while some may dev N/Synd. -Rapidly Progressive a.k.a Ellis type 1 nephritis or crescentic nephritis: Xterized by sudden onset azotemia, oliguria & rapid progress to RF within 2-6mths.Prognosis is usually poor.

  4. -Chronic Glomerulo Nephritis: This type dev. Insidiously, may follow Acute nephritis, N/synd or isolated haematuria. There is usually irreversible Glom damage + progressive decline in GFR. 2.Based on Aetiology: -Hereditary/familial e.gAlportssynd, fabrysdz -Post infectious: >bacteria = streptococcus, staph. >viral = Hep.B, varicella, measles, >parasitic =plasmodium malariae, schistosomiasis,toxoplasma, onchocercavolvolus, loiasis -Metabolic/Toxic =DM,Hg,Trimethadone -Systemic dz =SLE, HenochSchoenleinpurpura (anaphylactoidpurpura) -Coagulopathies = DIC -Malignancies = Leukemia, Hodgkin Lymphoma -Radiation = Radiation Nephritis • Low grade sepsis/

  5. >Parasitic = P.malariae, Schistosoma,Toxoplasma onchocerca, loiasis >Met./Toxic = D/M, Hg, Trimethadone >Systemic Dz = SLE, anaphylactoidpurpura (HSP) >Coagulopathies =DIC >Malignancies = Leukemia,Hodgkinymphoma >Radiation =Radiation Nephritis >Low grade Sepsis/SABE = Shunt Nephritis

  6. 3.Based on Renal Biopsy: Morphological classification is based on light mcpy, e-mcpy and immuno fluorescence. >minimal change >Focal glomerulosclerosis >membranous nephropathy >Proliferative GN. Proliferative GN =5 sub grps

  7. 1.Minimal Change GN: light mcpy -normal. Immuno fluorescence is negative. E-mcpy –fusion of epith foot processes Aetiology- Idiopathic. 2.Focal glom. Sclerosis (FGS): Glom. Lesions are focal and segmental in distributn

  8. FGS contd Immuno fluorescence is negative wt some segmental C3 or IgM deposits. Proteinuria > non selective.Runs a progressive course. E.gHeroine addiction. 3.Membranous nephropathy(DiffuseMembs.GN) Diffuse Uniform Thickening of all glom Cap. walls Immune compxdep in sub epith aspect of the cap BM.,SLEe.g >Hep.B,Qtan.malaria,SLE etc

  9. contd 4.Proliferative GN: Xterized generally by >Proliferation of mesangium,endothelium & epithelial cells. a) Membrano proliferative(diffse. mesangio-cap) Xterized by duplication of glom Bm giving a double contour (Tramline appearance)e.g SCD, neoplasm. b)Diffuse edocapillary GN (acute exudative).

  10. Diff. Endocap. contd The BM is normal There is a generalized & diffse. Prolifn. Of the capillary lumen. E.g B-haem.strep, staph, strep viridans c)Focal segmental prolif.GN:Prolif. Of mesangial & endoth. Cells obstructing cap. Loop in a segmt. of glom. Imm.flurescence>immun.glbs & complemts.e.g SLE,SABE,HSP.

  11. contd d)Crescentic GN(rapidly progressive GN): Show epith crescents in the bowman cap in 70-95% of glom.e.g some SABE,HSP,PSGN. e) Mesangio proliferative GN:prolif of mesangial cells wt little or no inc. in mesangial matrix e.gIgAneph, Lupus, resolving PSGN. 5.Quartan malaria:Thickn of cap walls of glom tuft, extensive mesangial sclerosis or segtscls. In 1/3 of all glom (if < severe)

  12. Acute GN classically manifests as acute nephritic synd. Other modes of presentation include : • nephrotic syndrome • Isolated haematuria • Symptomless proteinuria • HTN encephalopathy • CCF • ARF

  13. Acute Post-Streptococcal GN(APSGN) This is the prototype for acute proliferative GN. Various orgs Including bact, viruses etc are implicated in its etiology, top of which is Grp. A- b-haem. Strep. Neph’genic strains in 2 most common assoc ds. M type 1,3,4,12,25,49 in pharyngitis M type 2,49,55,57,60 in Pyoderma

  14. Epidermiology It is a dz of children and young adults.Peak age is 3-5yrs, more common in males. In the tropics APSGN is mainly 2ry to skin infxn wt scabies wt 2ry bact.(strep) infxn. 2 peaks are seen, june/july (peak of rainy season) & dusty harmattan season. It may occur sporadically or as regional epidermic usu. 2ry to pyoderma r/l strains. Most affected children are low socioeconomic grps. Some maybe frm high social class.

  15. Pathogenesis APSGN is basically an immune complex mediated GN. Recent studies by Peake et al suggest that nephritic strep. Assoc. protein NSAP wch is a streptokinasecan activate complement in vitro. It is thot that strep. Ag gets deposited in the glom. & Stim. fixatn of complement. At least 2 Ags. Isolated from strep, namely: zymogen precursor of exotoxin& glyceraldehydePhos. Dhasehave particular affinity for the glom & are known to induce Ab response causing activation of various pro-inflam mediator pathways in both glom and infilterating cells.

  16. Pathophysiology *Glom inflam >>Glom Cap obstn & dec. perm. Of glom. Bm>> dec. GFR>> renal retension>> if severe>>Azotemia, Acidemia,hyperK+, hyperP’temia. Glom inflam>>h’maturia & P’nuria *dec. distal deliv. Of Na+>>distal reabsptn of Na+ & plasma vol expansion>>HTN, * Inc. distal fluid & solute reabsorptn>> Oliguria, Pulmcongestn,oedema.Nb. Anemia is n’cytic & n’chromic 2ry to volexpsn & hemodiln.

  17. Pathology • In APSGN on light mcpy glom are enlarged and ischaemic wt obliteration of cap lumen leading to bloodless glom. Mesangial cell prolif wt infiltratn of neutrophils. • Immunoflorescence staining show;fine granular staining for IgG,C3&C1q along the cap walls • E mcpy reveals xteristic sub epith. “lumpy-bumpy” electron dense deposits on sub epith side of the cap Bm.

  18. Clinical features Latency from infxn to onset of symptoms -1-2wks for pharyngitis • 3-6wks for pyoderma. c/o sudden onset periorbitaloedema worse a.m Scanty (oliguria) wt smoky or cola color urine. Gross hematuria & edema are commonest c/o. HTN (70%),CCF, HTNsive encephalopathy, maybe Diln. anaemia.HTN & Edema are < freq in caucasians.

  19. Clin. features contd • Nb: assymptomatic cases are frequent.

  20. Investigation contd FBC: ESR raised wt mild n’chromic anemia(diln) WBC is within normal Proteinuria is mild-mod(1+-2+) excpt those wt NS(3+-4+). In unRx cases throat swab yield strep in abt 33% Antibody tests: Inc titre of ASO: rise is good after pharyngitis but poor after pyodermabcos some skin lipids are thot to interfere wt the test.Nb: maybe rsed in up to 20% of healthy children. Antihyaluronidase & anti Dnase B are raised.A rpt showing rising titre after 2-3wks is suggestive. Dec. C3 complement in >90% for the First 2wks. C3 normalises by 8wks.C3 is deposited in glom bm thus serum level falls.

  21. Inv. contd S/E/U/C: In the Oliguric phase, azotemia occurs wt rise in urea,cr, and k+. With onset of diuresis S/E/U/C normalizes excpt. in cases that progress to renal failure. Xray chest- evidence of pulm congestion. Abd US, shows norm to slightly bil.enlarged kidneys

  22. Indications for Renal Biopsy in AGN • Oliguria, HTN, azotemia persisting >2wks • Macroscopic hematuria persisting >4wks • Low C3 persisting > 8wks • Nephrotic range proteinuriabeyound 8wks • Assoc systemic features e.g rash, Jt. Pains, hepatosplenomegaly, persistent fever.

  23. Treatment Patients wt mild oliguria and normal BP can be Rx from home. In those wt HTN that need close attn to BP & diet hosp admsn is essential. Bed rest indicated as and when needed. Rx is essentially supportive. There are essentially 2 phases, an initial oliguricanuric phase followed 10-14days later by a diuretic phase. Diet/Fluid: In the initial stages of oligoanuria intake of salt & K+ to be restricted till S/E/U/C normalise & U.O improves. Reduce fluid intake to insensible loss plus previous 24hrs output in the Oliguric phase.

  24. Treatment contd Once edema resolves & u.o improves salt restrictn is gradually relaxed and fluid intake relaxed. Calorie is not restricted but protein should be made up of 60-70% high biological value type. In cases that dev pulm edema, I.V frusemide & IPPV are useful. In cardiogenic shock dopamine or dobutamine can be used.

  25. Txcontd Hypertension can be Rx with ACEI, Nifedipine 0.25-1mg/kg/day divided in 2 doses. Alpha methyl dopa (aldomet) can also be used. HTNsive encephalopathy-I.V frusemide + oral nifedipine. In refractory cases Nitroprusside as infusion is useful. In hyperkalemia, can be Rx wt I.V Ca gluconate, I.V NaHC03. I.V gluc wt insulin, neb. salbutamol or K+ xchange resin or dialysis depending on severity.

  26. Txcontd Antibiotics are indicated if the pt has any active infection or to prevent spread to contacts but does not influence course of illness. Course and Prognosis: Edema usually resolves by 10days & Bp usually normal by 2wks.Gross haematuriadissappears by 4wks but may be aggravated by inc physical activity. Mcpichematuria may persist for 1-2yrs. C3 level is normal in >95% by 10wks.Recurrence is rare bcos immunity to strep. M protein is type specific & long lasting &nephritogenic serotypes are ltd in no.